Brain Abscess in Emergency Medicine Clinical Presentation

Updated: May 18, 2017
  • Author: Naomi George, MD; Chief Editor: Jeter (Jay) Pritchard Taylor, III, MD  more...
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The natural history of brain abscess ranges from indolent to fulminant. The clinical presentation is dependent on multiple factors, including the location, size, and age of the lesion(s). The microbiology of the infection, the host’s immune status, and the mode of acquisition all contribute to the presentation.

The classic clinical triad of fever, headache, and focal neurologic deficit is present in less than 20% of cases. [16] Typically, clinical manifestations of brain abscess are due to local effect or mass effect and often are not heralded by signs and symptoms of systemic infection. [13, 22, 26, 37] When brain abscess is caused by direct spread of infection, symptoms often localize in predictable patterns; for example, otogenic infections are associated with cerebellar and temporal abscess, while sinus infection may lead to abscess in the frontal lobes. [1]

Headache is the most common presenting symptom and is observed in an average of 50-75% of patients. [2, 22] The headache is often nonspecific and may range from mild to severe and focal or generalized. Rupture of the abscess into the ventricular space may present as a sudden worsening of the headache and is often associated with high mortality. [38]

Fever is present in less than 50% of cases and may be particularly unreliable in patients with HIV infection or compromised immunological function. [39]

Focal neurological deficit such as hemiparesis or aphasia is present in 20-57% of patients and may correlate with the area of infection. [13, 37] Third or sixth cranial nerve palsies, anisocoria, or papilledema should all prompt concern for increased intracranial pressure and impending herniation.

Neck stiffness and meningeal signs have been reported in 25% of presentations [39, 40] ; when present, especially if associated with sudden worsening of headache, these signs may herald abscess rupture and subsequent poor outcome. [41]

Nausea and vomiting have been reported anywhere from 29-85% of cases, and the sign lacks sensitivity. [9, 11]

Seizure has been reported from 7–25% of patients in case series. [2, 10, 22]

Mental status changes are a common, but insensitive, marker. Glasgow Coma Scale score was less than 15 upon admission in 54% of patients in one large series. [39]



Initial manifestations of brain abscess may be nonspecific, and, therefore, delay in diagnosis is common. Mean time from symptom onset to diagnosis is 2 weeks. [42] Symptoms often correspond to increased intracranial pressure or local disruption of brain parenchyma. A thorough physical examination must include inspection of the external and middle ear, as well as inspection of the mastoid bone, sinuses, and dentition.

Fever may be present in approximately half of all presentations and does not reliably aid diagnosis or exclusion. [39]

Focal neurological deficits may be present in 40-60% of patients and may correlate with the area of infection. [2, 37, 39] If the affected brain region(s) has redundant functions with an unaffected area, then focal deficits may more difficult to recognize.

Brainstem abscess may lead to facial weakness or hypothalamic dysfunction. Cerebellar abscess may cause nystagmus, ataxia, or dysmetria. Occipital abscess may cause neck rigidity. Temporal lobe abscess may be associated with headache, visual defects, or dysarthria. Frontal abscess may be associated with motor, sensory disorders, or headache.

Lethargy may be a sign of global cerebral edema and should prompt concern for increased intracranial pressure and impending herniation.

Neck stiffness and meningeal signs have been reported in 25% of presentations. For patients who display Kernig and Brudzinski signs, with concomitant neurological deficits, a careful evaluation should be conducted for brain abscess. [39, 40]

Seizures have been reported in 7-25% of patients and may be generalized or focal, but they are more likely generalized. [2, 22, 37]

Mental status changes are a common but insensitive finding. [8, 10]

Third or sixth cranial nerve palsies, anisocoria, and papilledema may also be indications of increasing pressure and may indicate that the disease process has caused substantial edema either during the cerebritis stage or as a periabscess inflammatory response [43] ; therefore, a cranial nerve and funduscopic examination should be performed. A bedside ocular ultrasound is a reasonable adjunct to funduscopic examination to assess for increased intracranial pressure.

Infants may present with irritability or seizure. Examination must evaluate for bulging fontanels and should include measurement of head circumference. [44]



The microbiological causes of brain abscess are highly variable and depend on the mode of acquisition, as well as host factors such as age, immune status, and geographic location. In up to 25% of cases, no underlying etiology is found. [2] Many infections may be polymicrobial. [45] In immunocompetent hosts, abscesses are largely bacterial in etiology.

Direct extension

When the mode of acquisition is via direct extension, polymicrobial infections are common, occurring in approximately 20-25% of cases; these may involve aerobes and anaerobes, reflecting closely the flora of the contiguous site. [22, 37]

Aerobic and anaerobic streptococci are the most common isolates, found in approximately 70% of cases of bacterial brain abscess, and are frequently a component of mixed infections. [26] Streptococcus milleri is a particularly common isolate because its proteolytic enzymes can effectively necrose tissue and lead to the formation of abscesses. [46] In addition to Streptococcus species, site-specific pathogens include the following:

  • Otitis media and mastoiditis: Bacteroides, Enterobacteriaceae, Pseudomonas, Fusobacterium, Prevotella, Peptococcus, Pseudomonas, and Propionibacterium
  • Paranasal sinusitis: Bacteroides, Enterobacteriaceae, Staphylococcus aureus, Fusobacterium, and Haemophilus
  • Odontogenic infection: Fusobacterium, Prevotella, Actinomyces, and Bacteroides

Brain abscesses that result from hematogenous spread are often multiple, poorly encapsulated, and found in the territory of the middle cerebral artery. These abscesses often involve bacteria from the source infection, as in the following:

  • In pulmonary infections, common organisms are Streptococcus species , Fusobacterium species, anaerobic gram-negative bacilli, and aerobic and anaerobic streptococci. Infections with Actinomyces species and Nocardia species have been documented.
  • In bacterial endocarditis, the most common organisms are Streptococcus viridans, Streptococcus anginosus, and Streptococcus intermedius.
  • Congenital heart disease, as well as patent foramen ovale and other shunts, including intrapulmonary shunts, predispose to intracerebral spread of bacteremia. [47] Typically, cultures grow Streptococcus species. Evidence suggests that the severity of the grade of right-to-left intrapulmonary shunts is strongly associated with the prevalence of cerebral complications, such as brain abscess. [48]
  • Intra-abdominal infections and genitourinary tract infections are another source of hematogenous spread of bacteria. These infections can be caused by aerobic or anaerobic pathogens, which usually reflect colonic or genitourinary flora. [2] Frequent constituents include anaerobic streptococci, Bacteroides, (including Bacteroides fragilis), Escherichia coli, Proteus, Salmonella, Enterobacter, Prevotella, Propionibacterium, Eubacterium, Fusobacterium, and Actinomyces. Brain abscesses infected with Klebsiella pneumoniae in patients with primary liver abscesses have been described in Asia. [49, 50]
  • Skin infections can also lead to bacteremia, which can cause brain abscess. In addition to Streptococcus species, Staphylococcus aureus is frequently implicated.

Trauma and procedures

Penetrating intracranial trauma may be complicated by brain abscess with S aureus, coagulase-negative staphylococci, Pseudomonas aeruginosa, Enterobacter species, Enterobacteriaceae species , and Clostridium species.

Though less common, neurosurgical procedures may be complicated by similar infections. In particular, methicillin-resistant S aureus (MRSA) infection should be considered in neurosurgical patients, and treatment with antimicrobials must take into account CNS penetration. [51]

Rare cases of brain abscess after endoscopic procedure, tongue piercing, dental braces, near drowning, and foreign body aspiration have been documented. [52, 53, 54, 55, 56, 57, 58]


In immunocompromised hosts, causes of brain abscess may differ and could be the result of either opportunistic or bacterial infections. In addition to transplantation patients and those living with HIV/AIDS, individuals with alcoholism, diabetes, or long-term steroid use may be at increased risk for the development of brain abscess. [10]

Transplant organ recipients have a higher incidence of fungal infection from Aspergillus, Candida, Cryptococcus, Enterobacteriaceae, and Mucorales species. However, these patients may also have opportunistic infection with Toxoplasma gondii or Nocardia species. [59]

HIV/AIDS patients with impaired cell-mediated immune response are at a particularly high risk of developing abscesses infected with T gondii, Mycobacterium species, Cryptococcus neoformans, or Listeria monocytogenes infection. Additionally, tuberculosis should be considered in this population. [24]

Neutropenic patients are at risk for infection with aerobic gram-negative bacilli, as well as infection with Aspergillus, Mucorales, and Candida species.

Long-term corticosteroid use predisposes to increased risk of bacterial abscess. The incidence of brain abscess colonized with Listeria is elevated in patients on long-term steroid use and carries an elevated risk of mortality compared with brain abscess colonized with other bacterial pathogens. [60]

Pediatric patients

Pediatric patients remain a special subgroup. although brain abscess is increasingly rare in infants and children, the proportion of abscesses found in immunocompromised pediatric patients is increasing, whereas improved detection and management of otogenic infection has led to a decrease in abscesses due to direct extension of infection. [36, 44] Of note, the etiology of brain abscess in this population is more likely due to congenital cyanotic heart disease. [61] Citrobacter koseri, a gram-negative bacillus, has a strong propensity to form cerebral abscesses, and multiple case reports have documented cases in infants and children. [62, 63]

Mycotic, protozoal, and helminthic infections

Several mycotic, protozoal, and helminthic infections may be endemic in certain regions. For example, Latin American populations have higher rates of neurocysticercosis from Taenia solium infection, [64] while countries with endemic HIV/AIDS and tuberculosis experience higher rates of tubercular brain abscess. [65] Parasites are the most frequent cause of abscess in individuals who have lived in or emigrated from low-resource settings. Note the following:

  • Mycoses: Histoplasma capsulatum, Blastomyces dermatitidis, and Coccidioides immitis
  • Protozoal: Trypanosoma cruzi, Entamoeba histolytica, Schistosoma species, and Paragonimus species
  • Helminthic: Neurocysticercosis caused by the larval form of T solium

Other etiologies

Other etiologies of brain abscess include formation after meningeal infection. Although this mode of infection is rare, it is occurs more commonly in children, especially when facultative gram-negative organisms are suspected. [66] Additionally, brain abscess has been seen in the setting of intracranial hemorrhage, as well as intracerebral neoplasm. Patients with a history of intravenous drug abuse have an increased risk of infection. [67]